The central nervous system seems to play an important role in the pathogenesis of essential hypertension. The neural mechanisms involved are still not well understood. By interfering with baroreceptor reflexes experimental models of neurogenic labile hypertension have been developed. However, it has been difficult to obtain sustained hypertension. Furthermore, the lesions used in those models were rarely seen in human pathology and acutely interfered with homeostatic mechanisms in contrast to the progressive development of essential hypertension in the human. In patients with arterial hypertension who underwent posterior fossa exploration for glossopharyngeal neuralgia, we found tortuous vertebral or postero inferior cerebellar artery compressing the entry zone of IXth and Xth cranial nerves (carrying baroreceptor information to the nucleus tractus solitarius) into the medulla oblongata. Mobilization of the artery reduced hypertension in those patients. The objectives of our research are to 1) develop an experimental model of chronic neurogenic hypertension which imitates vascular cross-compression of the entry zone of cranial nerves IXth and Xth into the medulla, 2) to study the neuroanatomical, neurophysiological and biochemical changes underlying the development of neurogenic hypertension, and 3) to investigate whether on initial period of labile neurogenic hypertension will lead to established hypertension. An animal model has been designed in which a pulsating balloon simulating the ectatic vertebral artery is implanted lateral to the inferior olive and immediately anterior to the rootlets of IXth and Xth cranial nerves. Arterial pressure and heat rate are continuously monitored together with electrocardiogram and cardiac output determinations. Baroreceptor function is tested by plotting the change of pulse rate with the rapid rise in blood pressure induced by neo-synephrine. The reversibility of the changes when the balloon pulsation is discontinued is studied. Electrophysiological studies are performed to discriminate whether there is dysfunction of the afferent, efferent or central components of the baroreceptor reflex arc. Pharmacological tests and study of plasma levels of renin, nor-adrenalin and ADH will provide further information. In chronic experiments hemodynamic changes in the unanesthesized animal, and possible establishment of permanent hypertension will be studied. Finally, anatomic (Text Truncated -Exceeds Capacity)